Chapter title |
Cardiovascular and Hemostatic Disorders: SOCE and Ca2+ Handling in Platelet Dysfunction
|
---|---|
Chapter number | 23 |
Book title |
Store-Operated Ca²⁺ Entry (SOCE) Pathways
|
Published in |
Advances in experimental medicine and biology, January 2017
|
DOI | 10.1007/978-3-319-57732-6_23 |
Pubmed ID | |
Book ISBNs |
978-3-31-957731-9, 978-3-31-957732-6
|
Authors |
Jose J. Lopez, Gines M. Salido, Juan A. Rosado |
Abstract |
Among the Ca(2+) entry mechanisms in platelets, store-operated Ca(2+) entry (SOCE) plays a prominent role as it is necessary to achieve full activation of platelet functions and replenish intracellular Ca(2+) stores. In platelets, as in other non-excitable cells, SOCE has been reported to involve the activation of plasma membrane channels by the ER Ca(2+) sensor STIM1. Despite electrophysiological studies are not possible in human platelets, indirect analyses have revealed that the Ca(2+)-permeable channels involve Orai1 and, most likely, TRPC1 subunits. A relevant role for the latter has not been found in mouse platelets. There is a body of evidence revealing a number of abnormalities in SOCE or in its molecular regulators that result in qualitative platelet disorders and, as a consequence, altered platelet responsiveness upon stimulation with multiple physiological agonists. Platelet SOCE abnormalities include STIM1 and Orai1 mutations. This chapter summarizes the current knowledge in this field, as well as the disorders associated to platelet SOCE dysfunction. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Unknown | 12 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Researcher | 3 | 25% |
Professor > Associate Professor | 2 | 17% |
Student > Master | 2 | 17% |
Professor | 1 | 8% |
Unspecified | 1 | 8% |
Other | 1 | 8% |
Unknown | 2 | 17% |
Readers by discipline | Count | As % |
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Nursing and Health Professions | 1 | 8% |
Unspecified | 1 | 8% |
Agricultural and Biological Sciences | 1 | 8% |
Other | 1 | 8% |
Unknown | 2 | 17% |